Essay/Term paper: Alzheimer's disease

Essay, term paper, research paper:  Psychology

ALZHEIMER'S DISEASE


We are currently living in the age of technology. Our advancements in the
past few decades overshadow everything learned in the last 2000 years. With the
elimination of many diseases through effective cures and treatments, Canadians
can expect to live a much longer life then that of their grandparents. In 1900
about 4% of the Canadian population was over the age of 65. In 1989 that figure
tripled to 12% and the government expects that figure to rise to 23% by the year
2030 (Medical,1991,p.13). This increase has brought with it a large increase in
diseases associated with old age. Alzheimer's dementia (AD) is one of the most
common and feared diseases afflicting the elderly community. AD, once thought to
be a natural part of aging, is a severely debilitating form of mental dementia.
Although some other types of dementia are curable or effectively treatable,
there is currently no cure for the Alzheimer variety.
A general overview of Alzheimer's disease including the clinical
description, diagnosis, and progression of symptoms, helps one to further
understand the treatment and care of patients, the scope of the problem, and
current research.
The clinical definition of dementia is "a deterioration in intellectual
performance that involves, but is not limited to, a loss in at least 2 of the
following areas: language, judgement, memory, visual or depth perception, or
judgement interfering with daily activities" (Institute,1996, p.4).
The initial cause of AD symptoms is a result of the progressive
deterioration of brain cells (neurons) in the cerebral cortex of the brain. This
area of the brain, which is the largest and uppermost portion, controls all our
thought processes, movement, speech, and senses. This deterioration initially
starts in the area of the cortex that is associated with memory and then
progresses into other areas of the cortex, then into other areas of the brain
that control bodily function. The death of these cells causes an interruption of
the electrochemical signals between neurons that are a key to cognitive as well
as bodily functioning.
Currently AD can only be confirmed at autopsy. After death the examined
brain of an Alzheimer victim shows two distinct characteristics. The first is
the presence of neuritic plaques in the cerebral cortex and other areas of the
brain including cerebral blood vessels. These plaques consist of groups of
neurons surrounded by deposits of beta-amyloid protein. The presence of these
plaques is also common to other types of dementia.
The second characteristic, neurofibliary tangles, is what separates AD from
all other forms of dementia. Neurofibliary tangles take place within the
disconnected brain cells themselves. When examined under a microscope diseased
cells appear to contain spaghetti-like tangles of normally straight nerve fibers.
The presence of these tangles was first discovered in 1906 by the German
neurologist Alois Alzheimer, hence the name Alzheimer's disease.
Although the characteristics listed above are crucial to the diagnosis of
AD upon death, the clinical diagnosis involves a different process. The
diagnosis of AD is only made after all other illnesses, which may have the same
symptoms, are ruled out. The initial symptoms of AD are typical of other
treatable diseases therefore doctors are hesitant to give the diagnosis of
Alzheimer's in order to save the patient from the worsening of a treatable
disease through a misdiagnosis. Some of the initial symptoms include an
increased memory loss, changes in mood, personality, and behavior, symptoms that
are common of depression, prescription drug conflict, brain tumors, syphilis,
alcoholism, other types of dementia, and many other conditions.
The onset of these symptoms usually brings the patient to his family doctor.
The general practitioner runs a typical battery of urinalysis and blood tests
that he sends off to the lab. If the tests come back negative, and no other
cause of the symptoms is established, the patient is then refereed to a
specialist. The specialist, usually a psychiatrist, will then continue to rule
out other possible illnesses through testing. If the next battery of tests also
comes back negative then the specialist will call on a neurologist to run a
series of neurological examinations including a PET and CAT scan to rule out the
possibility of brain tumors. A spinal tap is also performed to determine the
possibility of other types of dementias. The patient will also undergo a
complete psychiatric evaluation. If the patient meets the preliminary criteria
for AD an examination of the patients medical history is also necessary to check
for possible genetic predispositions to the disease.
The psychiatric team finally meets with the neurological team to discuss
their findings. If every other possible disease is ruled out, and the results of
the psychiatric evaluation are typical to that of a person with AD, the
diagnosis of Alzheimer's disease is given.
The initial symptoms of AD are usually brushed off as a natural part of
aging. The myth that a person's memory worsens over time is just that - a myth
(Myers,1996, p.100-101). AD's victims are mostly over the age of 65 and many
delay treatment by attributing their problems to age. A victim might forget a
well known phone number or miss an important appointment. These symptoms
eventually escalate to the total disintegration of personality and all patients
end up in total nursing care.

In descending order, the patient goes from (1) decreased ability to
handle a
complex job to (2) decreased ability to handle such complex activities
of daily
life as (3) managing finances, (4) complex meal preparation and (5)
complex
marketing skills.Next comes (6) loss of ability to pick out clothing
properly, (7)
or to put on clothing properly, followed by (8) loss of ability
to handle
the mechanics of bathing properly. Then (9) progressive
difficulties with
continence and (10) toileting occur, followed by (11) very limited speech
ability
and (12) inability to speak more than a single word. Next comes (13)
loss of
ambulatory capability. Last to go are such basic functions as (14) sit
up, (15)
smile and (16) hold up one's head (Brassard,1993,p.10).

The average time from diagnosis to inevitable death is 8 years. The family
of the victim is usually able to care for the victim for an average period of
about 4 years (Alzheimer's, 1996,p.44).During the progression of the disease
between 10% and 15% of patients hallucinate and suffer delusions, 10% will
become violent and 10% suffer from seizures (Alzheimer's,1996,p.46).
Once a person is diagnosed as having AD, an assessment is made of the
disease's stage of progression and of the strengths and weaknesses of the victim
and the victim's family. There are different types of assessments available to
evaluate the level of dysfunction of the patient. Based on one of these
assessments a care plan is put together by a team consisting of a family member,
a paid or unpaid care provider, and the victim's physician. Throughout the
progression of the disease, and depending on the needs of the patient, a wide
range of expensive medication, such as psychoactive drugs to lift depression and
sedatives to control violence, may be required.
Unfortunately, although a wide range of treatments have been tested, most
prove to be ineffective. At the beginning of the disease the family is able to
look after the patient without much effort. Frequently families will hire a care
giver in order to alleviate some of the work.
Simple changes in the home can make life much easier for the sufferer, help
them keep their self esteem, and prolong their stay at home. Examples of low-
cost modifications to the environment include reducing the noise levels in the
home (telephones, radios, voices, etc.); avoiding vividly patterned rugs and
drapes; placing locks up high or down low on doors leading outside (AD sufferers
are known to wander off); clearing floors of clutter; reducing the contents of
closets in order to simplify choices (Alzheimer,1992, p.17). These costs are
paid for by the victim's family. Many of these, and other more expensive
modifications are introduced in long-term care settings. They help in
maintaining the safety and security of the victim as well as reducing their
confusion.
The patient's and the family's condition should be assessed every six
months (Alzheimer,1992, p.21). In response to constantly changing needs, the
aspects of care must be constantly modified. Other issues that usually arise
during the care of the patient are assessment of the competence of the victim,
power of attorney, and response to and prevention of abuse (Aronson,1988, p.124).
Eventually the victim's condition deteriorates to the point where home care is
no longer possible and they must be moved to a long-term care facility.
In Canada care, support and information for victims and their families
comes from the health care system and the Alzheimer's Society of Canada. The
care giver must obtain information and education about the disease in order to
effectively care for the victim. During the course of the disease victims might
wander, hallucinate, become suspicious. This behavior can place a large strain
on the care giver as well as causing depression and deterioration of their own
health (Aronson,1988, p.132). An AD support group is crucial to alleviating some
of the stress on the care giver. Through a support group the care giver is given
the emotional and practical help needed to accomplish the large task of looking
after the victim for as long as possible.
Currently there are 300,000 persons in Canada with AD. This figure is more
than that of Parkinson's disease, cancer and multiple sclerosis combined. With
continuous growth in the percentage of Canadians over the age of 65, this
figure could hit 700,000 by the year 2020 (Carlton,1996,p.17). These large and
increasing figures translate into a large burden on the health care system.

Even when using the most conservative estimates of the average number of
years
spent in an institution and the number of afflicted Canadians, the costs to
health
care are immense. At $33,000 (1989) per patient per year in an
institution and
with an average stay of three years until death, the cost of AD will amount
to $3
billion over the next three years; and if the entry into the disease
state remains
constant, it will cost the Canadian taxpayer [an added] $1 billion per year
thereafter.(Brassard,1993,p.11)

There have been many studies that conclude that the number of incidences of
AD is on the rise. A very high incidence was reported in a U.S. survey conducted
in East Boston by the Harvard Medical school. It showed the incidence of AD to
be 3% for people between the ages of 65-74, 18.7% for those between 75-84, and
47.2% for those over 84 (Evans,1989,p.4).
AD is a democratic disease. It affects persons of both sexes and all
races and ethnic backgrounds. The major risk factors for AD are age and heredity.
Persons with a high incidence of AD in their family history are most succeptable.

A specific subtype of AD exists that is solely connected to heredity. This
subtype is known as Familial Alzheimer's disease (FAD). FAD is also known as
Early Onset Alzheimer's disease, named so because its symptoms start to develop
much earlier than in the regular sporadic type. Only 5%-10% of all cases are of
this type. FAD is suspected when AD can be traced over several generations and
there is a history of, among previously affected family members, a similar age
of onset and duration of the disease ( usually 4 years ) . Approximately 50% of
the children of an affected parent go on to develop the disease
(Pollen,1993,p.89).
Much research has been conducted in an attempt to locate the gene that is
responsible for FAD. Currently, researchers have isolated genes 1, 14, and 21
(Alzheimer's,1996,p.36), however, the evidence still remains inconclusive
(Statement,1996, p.2). There is also a possibility that a specific genetic
mutation merely puts a person at risk to the disease and AD is triggered by an
external force e.g. a head injury.(Statement,1996,p.4). Finding the specific
location of the gene will pave the way for a diagnostic or even predictive test
for FAD. Similar genetic tests already exist for cystic fibrosis and muscular
dystrophy. Locating the AD gene will also allow scientists to study why the
particular gene is not functioning properly and may give clues to treatment and
cure. The long term goal of this research is the same as that of any other
genetic research and that is gene therapy - which is the possibility that
science could one day alter our genetic make-up.
The other much more common type of AD is Sporadic Alzheimer's Disease (SAD).
This includes all other types of the disease which are not linked to heredity.
Genetic research is also playing a major role in the progress towards a
diagnostic or predictive test for SAD. Recently, a gene involved in the
transport of cholesterol has been identified to be associated with AD.
Apolipoprotein E is located on chromosome 19 and seems to contribute to the
succeptability of a persons to AD (Statement,1996,p.6). The gene exists in three
different forms or alleles (Apo E 2,3,4) and each person has a combination of
two of the three. Thus an individual can have any one of the following
combinations: Apo E 2/2, 3/3, 4/4, 2/3/, 3/4 or 2/4. Researchers have found a
relationship between the number of copies of the 4 allele and the person's
probability of developing the disease.
















Source: Institute for Brain Aging

FIGURE 1 illustrates an analysis of the proportion of individuals remaining
normal at increasing ages for two, one, or zero copies of Apo E
4...For
example a 75 year old individual with the Apo E 4
genotype has
approximately a 20% chance of remaining normal; Apo E 3/4 or
2/4,
40%; 2/2, 3/3 or 2/3, a 75% chance. For many years, scientists believed
that aluminum was at the root of AD. High levels of aluminum were detected in
the areas surrounding the beta-amyloid plaques associated with neural atrophy
(Pollen,1990,p.77). Recently, however, this theory has been abandoned.
Scientists concluded that the build-up of aluminum was a direct result of the
wrongful use of a particular test agent employed in the studies (Brown,1992,
p.6).
Some of the current pursuits of research are in the areas of viral
infection, malfunction of the immune system, and chemical imbalances. One of the
hardest theories to disprove is that AD is the result of a slow acting virus
present at birth (Carlton,1996,p.13). Others believe that AD is an immune system
disorder. Support for this theory comes from the presence of beta-amyloid
plaques identical to those found in AD brains in the post mortem examinations of
immuno-deficiency disease victims (Alzheimer's,1996,p.22).
The detection of lower neurotransmitter substances such as acetylcholine,
serotonin, norepinephrine and somatostatin in AD sufferers forms the basis of
another theory that says AD is brought on by a chemical imbalance in the brain.
Treatment of patients with drugs that block the break down of neurotransmitter
substances in the brain have been met with limited success (Brassard,1993,p.16).

AD is an enormous social and economic problem. As the population ages, the
number of victims will steadily increase, imposing a massive burden on the
health care system. Until a cure and effective treatment are found AD will
remain a terrible disease that slowly eats away at that which is the very
essence of a person, their mind, leaving in its wake a mere empty shell of that
person. It takes away from all of us the insightful wisdom of society's most
prized possession - the elderly.

References

Alzheimer Society of Canada.(1992).Guidelines for Care.Toronto: Alzheimer
Society of Canada.

Alzheimer's Disease Education and Referal
Centre.(1996).Internet.http:\www.alzheimers.
org/adear.drct.txt

Aronson, Miriam.(1988).Understanding Alzheimer's disease.New York: Scribner's.

Brassard, Daniel.(1993).Alzheimer's Disease.Ottawa: Library of Parliament,
Science and
Technology Division.

Brown, Phyllida.(1992, November 7).Alzheimer's May Not be Linked to Aluminum.New
Scientist
Supplement,p.6.

Carlton University Department of Health Sciences
Freenet.(1996).Internet.http:\www.nct.carlton
ca/fp/social.services/alzheimer/disease.dir

Evans, Denis, et al.(1989).Prevalence of Alzheimer's Disease in a Community
Population of
Older Persons.Journal of the American Medical Association,272(15),1152.

Institute for Brain Aging.(1996).Internet.http:\www.128.200.55.17/aboutad.html

Medical Research Council of Canada.(1991).Presidents Report 1989-1990.

Myers, David.(1996).Exploring Psychology.New York: Worth.

Pollen, Daniel.(1990).Hannah's Heirs: The Quest For the Genetic Origins of
Alzheimer's
Disease.London:Oxford University Press.

Statement on Use of Apolipoprotein E Testing for Alzheimer's
Disease.(1996).American College of Medical Genetics/American Society of Human
Genetics Working Group on ApoE and Alzheimer's
Disease.Internet.http:\www.faseb.org/genetics/asng/policy/pot